Saturation divers regularly inspect North Sea installations, working at depth for periods of 12-16 days. Diver's hand is a particular problem in saturation diving, and there is no eVective protection or treatment available. This paper presents the occurrence of diver's hand and describes the disease in clinical and epidemiological terms. Three studies of diver's hand have been carried out, in 1990, 1994, and 1995. Most long term saturation divers have had diver's hand at some time in their professional career. Diver's hand seems able to occur without any previous skin symptoms, and divers without diver's hand can have several other skin symptoms during a saturation period. It is likely that diver's hand is a specific phenomenon associated with saturation diving.

Recent advances in submarine rescue systems have allowed a transfer under pressure of crew members being rescued from a disabled submarine. The choice of a safe decompression procedure for pressurised rescuees has been previously discussed, but no schedule has been validated when the internal submarine pressure is significantly increased i.e. exceeding 2.8 bar absolute pressure. This study tested a saturation decompression procedure from hyperbaric exposures up to 6 bar, the maximum operating pressure of the NATO submarine rescue system. The objective was to investigate the incidence of decompression sickness (DCS) and clinical and spirometric indices of pulmonary oxygen toxicity. Two groups were exposed to a Nitrogen-Oxygen atmosphere (pO2 = 0.5 bar) at either 5 bar (N = 14) or 6 bar (N = 12) for 12 h followed by 56 h 40 min resp. 60 h of decompression. When chamber pressure reached 2.5 bar, the subjects breathed oxygen intermittently, otherwise compressed air. Repeated clinical examinations, ultrasound monitoring of venous gas embolism and spirometry were performed during decompression. During exposures to 5 bar, 3 subjects had minor subjective symptoms i.e. sensation of joint discomfort, regressing spontaneously, and after surfacing 2 subjects also experienced joint discomfort disappearing without treatment. Only 3 subjects had detectable intravascular bubbles during decompression (low grades). No bubbles were detected after surfacing. About 40% of subjects felt chest tightness when inspiring deeply during the initial phase of decompression. Precordial burning sensations were reported during oxygen periods. During decompression, vital capacity decreased by about 8% and forced expiratory flow rates decreased significantly. After surfacing, changes in the peripheral airways were still noticed; Lung Diffusion for carbon monoxide was slightly reduced by 1% while vital capacity was normalized. The procedure did not result in serious symptoms of DCS or pulmonary oxygen toxicity and may be considered for use when the internal submarine pressure is significantly increased.

The acute effects of the beta 1-adrenoceptor inhibition by atenolol were investigated on conscious rats. Cardiac output and organ blood flow were measured by 15-microns radiolabelled microspheres during control and 20 min after administration of atenolol (1 mg/kg body wt). Arterial blood pressure and heart rate were measured continuously. Arterial blood gases and pH were determined immediately after the two microsphere injections and arterial blood samplings. The mean arterial blood pressure fell significantly shortly after the injection of atenolol and was reduced by 9% (p less than 0.02) after 20 min. Heart rate fell by 17% (p less than 0.05). The total peripheral vascular resistance increased by 25% (p less than 0.05). At the same time the arterial acid-base chemistry remained unaltered from the control. The cardiac output fell by 24% (p less than 0.05). Blood flow fell to all organs and tissues (0-67%) except to the brain, adrenals, liver, ears and diaphragm. The greatest decrease was seen in perfusion of the adipose tissue (67%) and of the spleen (60%), indicating that the blood flow to these organs are normally highly influenced by beta 1-adrenoceptor stimulation. The estimated work load of the heart was reduced by 20% which correlated well to a reduction of myocardial blood flow to the same degree.

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We do not recommend screening for patent foramen ovale in divers because the absolute risk of decompression illness is small and transcatheter closure is only indicated after decompression illness in some occupational divers.